SARS-CoV-2-induced amyloidgenesis : not one, but three hypotheses for cerebral COVID-19 outcomes
Autor(a) principal: | |
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Data de Publicação: | 2022 |
Outros Autores: | , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UFRGS |
Texto Completo: | http://hdl.handle.net/10183/256390 |
Resumo: | The main neuropathological feature of Alzheimer’s disease (AD) is extracellular amyloid deposition in senile plaques, resulting from an imbalance between the production and clearance of amyloid beta peptides. Amyloid deposition is also found around cerebral blood vessels, termed cerebral amyloid angiopathy (CAA), in 90% of AD cases. Although the relationship between these two amyloid disorders is obvious, this does not make CAA a characteristic of AD, as 40% of the non-demented population presents this derangement. AD is predominantly sporadic; therefore, many factors contribute to its genesis. Herein, the starting point for discussion is the COVID-19 pandemic that we are experiencing and how SARS-CoV-2 may be able to, both directly and indirectly, contribute to CAA, with consequences for the outcome and extent of the disease. We highlight the role of astrocytes and endothelial cells in the process of amyloidgenesis, as well as the role of other amyloidgenic proteins, such as fibrinogen and serum amyloid A protein, in addition to the neuronal amyloid precursor protein. We discuss three independent hypotheses that complement each other to explain the cerebrovascular amyloidgenesis that may underlie long-term COVID-19 and new cases of dementia. |
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Goncalves, Carlos Alberto SaraivaBobermin, Larissa DanieleSesterheim, PatríciaNetto, Carlos Alexandre2023-03-29T03:24:44Z20222218-1989http://hdl.handle.net/10183/256390001164293The main neuropathological feature of Alzheimer’s disease (AD) is extracellular amyloid deposition in senile plaques, resulting from an imbalance between the production and clearance of amyloid beta peptides. Amyloid deposition is also found around cerebral blood vessels, termed cerebral amyloid angiopathy (CAA), in 90% of AD cases. Although the relationship between these two amyloid disorders is obvious, this does not make CAA a characteristic of AD, as 40% of the non-demented population presents this derangement. AD is predominantly sporadic; therefore, many factors contribute to its genesis. Herein, the starting point for discussion is the COVID-19 pandemic that we are experiencing and how SARS-CoV-2 may be able to, both directly and indirectly, contribute to CAA, with consequences for the outcome and extent of the disease. We highlight the role of astrocytes and endothelial cells in the process of amyloidgenesis, as well as the role of other amyloidgenic proteins, such as fibrinogen and serum amyloid A protein, in addition to the neuronal amyloid precursor protein. We discuss three independent hypotheses that complement each other to explain the cerebrovascular amyloidgenesis that may underlie long-term COVID-19 and new cases of dementia.application/pdfengMetabolites. Basel. Vol. 12, no. 11 (Nov. 2022), 1099, 11 p.AmilóideCOVID-19SARS-CoV-2Doença de AlzheimerAmyloidAstrocyteFibrinSerum amyloid ASARS-CoV-2-induced amyloidgenesis : not one, but three hypotheses for cerebral COVID-19 outcomesEstrangeiroinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFRGSinstname:Universidade Federal do Rio Grande do Sul (UFRGS)instacron:UFRGSTEXT001164293.pdf.txt001164293.pdf.txtExtracted Texttext/plain44815http://www.lume.ufrgs.br/bitstream/10183/256390/2/001164293.pdf.txtcaec5112a329a2c82908035f0fecd09aMD52ORIGINAL001164293.pdfTexto completo (inglês)application/pdf7577881http://www.lume.ufrgs.br/bitstream/10183/256390/1/001164293.pdf9a0d1d6e5a53c9b49d070463bbc197c7MD5110183/2563902023-03-30 03:23:19.904167oai:www.lume.ufrgs.br:10183/256390Repositório de PublicaçõesPUBhttps://lume.ufrgs.br/oai/requestopendoar:2023-03-30T06:23:19Repositório Institucional da UFRGS - Universidade Federal do Rio Grande do Sul (UFRGS)false |
dc.title.pt_BR.fl_str_mv |
SARS-CoV-2-induced amyloidgenesis : not one, but three hypotheses for cerebral COVID-19 outcomes |
title |
SARS-CoV-2-induced amyloidgenesis : not one, but three hypotheses for cerebral COVID-19 outcomes |
spellingShingle |
SARS-CoV-2-induced amyloidgenesis : not one, but three hypotheses for cerebral COVID-19 outcomes Goncalves, Carlos Alberto Saraiva Amilóide COVID-19 SARS-CoV-2 Doença de Alzheimer Amyloid Astrocyte Fibrin Serum amyloid A |
title_short |
SARS-CoV-2-induced amyloidgenesis : not one, but three hypotheses for cerebral COVID-19 outcomes |
title_full |
SARS-CoV-2-induced amyloidgenesis : not one, but three hypotheses for cerebral COVID-19 outcomes |
title_fullStr |
SARS-CoV-2-induced amyloidgenesis : not one, but three hypotheses for cerebral COVID-19 outcomes |
title_full_unstemmed |
SARS-CoV-2-induced amyloidgenesis : not one, but three hypotheses for cerebral COVID-19 outcomes |
title_sort |
SARS-CoV-2-induced amyloidgenesis : not one, but three hypotheses for cerebral COVID-19 outcomes |
author |
Goncalves, Carlos Alberto Saraiva |
author_facet |
Goncalves, Carlos Alberto Saraiva Bobermin, Larissa Daniele Sesterheim, Patrícia Netto, Carlos Alexandre |
author_role |
author |
author2 |
Bobermin, Larissa Daniele Sesterheim, Patrícia Netto, Carlos Alexandre |
author2_role |
author author author |
dc.contributor.author.fl_str_mv |
Goncalves, Carlos Alberto Saraiva Bobermin, Larissa Daniele Sesterheim, Patrícia Netto, Carlos Alexandre |
dc.subject.por.fl_str_mv |
Amilóide COVID-19 SARS-CoV-2 Doença de Alzheimer |
topic |
Amilóide COVID-19 SARS-CoV-2 Doença de Alzheimer Amyloid Astrocyte Fibrin Serum amyloid A |
dc.subject.eng.fl_str_mv |
Amyloid Astrocyte Fibrin Serum amyloid A |
description |
The main neuropathological feature of Alzheimer’s disease (AD) is extracellular amyloid deposition in senile plaques, resulting from an imbalance between the production and clearance of amyloid beta peptides. Amyloid deposition is also found around cerebral blood vessels, termed cerebral amyloid angiopathy (CAA), in 90% of AD cases. Although the relationship between these two amyloid disorders is obvious, this does not make CAA a characteristic of AD, as 40% of the non-demented population presents this derangement. AD is predominantly sporadic; therefore, many factors contribute to its genesis. Herein, the starting point for discussion is the COVID-19 pandemic that we are experiencing and how SARS-CoV-2 may be able to, both directly and indirectly, contribute to CAA, with consequences for the outcome and extent of the disease. We highlight the role of astrocytes and endothelial cells in the process of amyloidgenesis, as well as the role of other amyloidgenic proteins, such as fibrinogen and serum amyloid A protein, in addition to the neuronal amyloid precursor protein. We discuss three independent hypotheses that complement each other to explain the cerebrovascular amyloidgenesis that may underlie long-term COVID-19 and new cases of dementia. |
publishDate |
2022 |
dc.date.issued.fl_str_mv |
2022 |
dc.date.accessioned.fl_str_mv |
2023-03-29T03:24:44Z |
dc.type.driver.fl_str_mv |
Estrangeiro info:eu-repo/semantics/article |
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info:eu-repo/semantics/publishedVersion |
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article |
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http://hdl.handle.net/10183/256390 |
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2218-1989 |
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001164293 |
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http://hdl.handle.net/10183/256390 |
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eng |
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dc.relation.ispartof.pt_BR.fl_str_mv |
Metabolites. Basel. Vol. 12, no. 11 (Nov. 2022), 1099, 11 p. |
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openAccess |
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